Ruminant animals are naturally infected with the pathogen Escherichia coli O157:H7, annually responsible for numerous meat recalls, foodborne illnesses and deaths. E. coli are equipped with the enzyme nitrate reductase, which not only enables this bacteria to respire anaerobically, but also converts chlorate to the toxic metabolite chlorite. This enzyme system is particular to only a few intestinal bacteria, therefore the vast majority are not affected by chlorate. Sodium chlorate has been shown to effectively decrease foodborne pathogens in several livestock species, including ruminants. However, because infection and proliferation of E. coli occurs primarily in the lower intestine, there is interest in “by-passing” the rumen, thereby, delivering chlorate directly to the largest population of pathogens. The objective of the current study was to evaluate the ability of an experimental sodium chlorate product (ECP II), designed to by-pass the rumen, in reducing fecal shedding and gut concentrations of E. coli O157:H7. Twenty crossbred mature ewes were adapted to a high grain ration and experimentally inoculated with E. coli O157:H7. Thirty-six hours following inoculation, sheep received in their feed one of the following ECP treatments: (1) control (CON), no chlorate; (2) 1 X (LOW); (3) 2 X (MED); and (4) 4 X (HIGH) where X=1.1 g chlorate ion equivalents/kg BW (five sheep per treatment). Fecal samples were collected every 12 h following inoculation and 24 h following the feeding of chlorate, all animals were euthanized and tissue samples and their respective contents collected from the rumen, cecum and rectum. The MED and HIGH chlorate treatments significantly reduced fecal shedding of E. coli O157:H7 compared to the CON treatment [1.53, 1.11, and 3.89 CFU/g feces (log 10), respectively]. Ruminal contents were similar among treatments, while chlorate tended to decrease ( P=0.08) and reduced ( P<0.05) E. coli O157:H7 populations in the cecum and rectum, respectively. Populations of generic E. coli in the cecal contents were numerically lower ( P=0.11) in the LOW treatment and tended to decrease ( P=0.06) in the MED and HIGH chlorate treatments, respectively. Fermentation profiles through the gastrointestinal tract were unaffected as indicated by slight, but not significant, changes in volatile fatty acids (VFA) profiles in sheep fed chlorate. Results from this study indicate that this experimental chlorate product, administered in the feed, was effective in reducing E. coli O157:H7 from the lower gut of sheep as evidenced by the lower cecal and rectal but not ruminal concentrations. Feeding chlorate may be an effective method to decrease E. coli O157:H7 populations in ruminant animals prior to slaughter.
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